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A nuclear export signal (NES) is a short target peptide containing 4 hydrophobic residues in a protein that targets it for export from the cell nucleus to the cytoplasm through the nuclear pore complex using nuclear transport. It has the opposite effect of a nuclear localization signal, which targets a protein located in the cytoplasm for import to the nucleus. The NES is recognized and bound by exportins.
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A nuclear export signal (NES) is a short target peptide containing 4 hydrophobic residues in a protein that targets it for export from the cell nucleus to the cytoplasm through the nuclear pore complex using nuclear transport. It has the opposite effect of a nuclear localization signal, which targets a protein located in the cytoplasm for import to the nucleus. The NES is recognized and bound by exportins.
NESs serve several vital cellular functions. They assist in regulating the position of proteins within the cell. Through this NESs effect transcription and several other nuclear functions that are essential to proper cell function.[1]The export of many types of RNA from the nucleus is required for proper cellular function. The NES determines what type of pathway the varying types of RNA may use to exit the nucleus and perform their function and the NESs may effect the directionality of molecules exiting the nucleus.[2]
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Mechanism[edit]
Nuclear export first begins with the binding of Ran-GTP (a G-protein) to exportin. This causes a shape change in exportin, increasing its affinity for the export cargo. Once the cargo is bound, the Ran-exportin-cargo complex moves out of the nucleus through the nuclear pore. GTPase activating proteins (GAPs) then hydrolyze the Ran-GTP to Ran-GDP, and this causes a shape change and subsequent exportin release. Once no longer bound to Ran, the exportin molecule loses affinity for the nuclear cargo as well, and the complex falls apart. Exportin and Ran-GDP are recycled to the nucleus separately, and guanine exchange factor (GEF) in the nucleus switches the GDP for GTP on Ran.
(draft of new text - (3/2))
Mechanism[edit]
Nuclear export first begins with the binding of Ran-GTP (a G-protein) to exportin. This causes a shape change in exportin, increasing its affinity for the export cargo. Once the cargo is bound, the Ran-exportin-cargo complex moves out of the nucleus through the nuclear pore. GTPase activating proteins (GAPs) then hydrolyze the Ran-GTP to Ran-GDP, and this causes a shape change and subsequent exportin release. Once no longer bound to Ran, the exportin molecule loses affinity for the nuclear cargo as well, and the complex falls apart. Exportin and Ran-GDP are recycled to the nucleus separately, and guanine exchange factor (GEF) in the nucleus switches the GDP for GTP on Ran.
mRNA Transport[edit]
During the processing phase of mRNA export, mRNA is covered with RNA-binding proteins, this yields ribonucleoprotein particles (mRNPs). Through the process, the correct assortment of proteins is necessary for the mRNPs eventual export. The heterodimeric export receptor yeast Mex67-Mtr2/human NXF1-NXT1 is the NES responsible for signalling the completion of the mRNP construction.This signal mediates the mRNPs movement out of the nuclear envelope through the NPC. The assembled mRNPs are directed out of the nucleus and into the cytoplasm by two DEAD-box ATPases. On the nucleus side is yeast Sub2/human UAP56 and on the cytoplasm side is the ATPase yeast Dbp5/human DDX19.[3]
Chemotherapy[edit]
The process of nuclear export is responsible for some resistance to chemotherapy drugs. By limiting a cells nuclear export activity it may be possible to reverse this resistance. By inhibiting CRM1, the export receptor, export through the nuclear envelope may be slowed. Survivin is a NES that inhibits cellular apoptosis. It interacts with the mitotic spindles during cellular division. Due to the usually rapid proliferation of tumour cells, survivin is more expressed during the presence of cancer. The level of survivin correlates to how resistance to chemotherapy a cancerous cell is and how likely that cell is to replicate again. By producing antibodies to target the NES survivin, apoptosis of cancerous cells can be increased.[4]
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- ^ Fukuda, Makoto; Asano, Shiro; Nakamura, Takahiro; Adachi, Makoto; Yoshida, Minoru; Yanagida, Mitsuhiro; Nishida, Eisuke (1997-11). "CRM1 is responsible for intracellular transport mediated by the nuclear export signal". Nature. 390 (6657): 308–311. doi:10.1038/36894. ISSN 0028-0836.
{{cite journal}}: Check date values in:|date=(help) - ^ Li, Zhengguo; Kearse, Michael G.; Huang, Chuan (2019-01-02). "The nuclear export of circular RNAs is primarily defined by their length". RNA Biology. 16 (1): 1–4. doi:10.1080/15476286.2018.1557498. ISSN 1547-6286. PMC 6380329. PMID 30526278.
{{cite journal}}: CS1 maint: PMC format (link) - ^ Xie, Yihu; Ren, Yi (2019-11). "Mechanisms of nuclear mRNA export: A structural perspective". Traffic. 20 (11): 829–840. doi:10.1111/tra.12691. ISSN 1398-9219.
{{cite journal}}: Check date values in:|date=(help) - ^ El-Tanani, Mohamed; Dakir, El-Habib; Raynor, Bethany; Morgan, Richard (2016-03-14). "Mechanisms of Nuclear Export in Cancer and Resistance to Chemotherapy". Cancers. 8 (3): 35. doi:10.3390/cancers8030035. ISSN 2072-6694. PMC 4810119. PMID 26985906.
{{cite journal}}: CS1 maint: PMC format (link) CS1 maint: unflagged free DOI (link)